RESUMO
This study examined the molecular mechanisms of methionine pathways in meat-type chickens where birds were provided with a diet deficient in methionine from 3 to 5 weeks of age. The birds on the deficient diet were then provided with a diet supplemented with either D,L-methionine or D,L-HMTBA from 5 to 7 weeks. The diet of the control birds was supplemented with L-methionine from hatch till 7 weeks of age. We studied the mRNA expression of methionine adenosyltransferase 1, alpha, methionine adenosyltransferase 1, beta, 5-methyltetrahydrofolate-homocysteine methyltransferase, 5-methyltetrahydrofolate-homocysteine methyltransferase reductase, betaine-homocysteine S-methyltransferase, glycine N-methyltransferase, S-adenosyl-L-homocysteine hydrolase and cystathionine beta synthase genes in the liver, duodenum, Pectoralis (P.) major and the gastrocnemius muscle at 5 and 7 weeks. Feeding a diet deficient in dietary methionine affected body composition. Birds that were fed a methionine-deficient diet expressed genes that indicated that remethylation occurred via the one-carbon pathway in the liver and duodenum; however, in the P. major and the gastrocnemius muscles, gene expression levels suggested that homocysteine received methyl from both folate and betaine for remethylation. Birds who were switched from a methionine deficiency diet to one supplemented with either D,L-methionine or D,L-HMTBA showed a downregulation of all the genes studied in the liver. However, depending on the tissue or methionine form, either folate or betaine was elicited for remethylation. Thus, mRNA expressions show that genes in the remethylation and transsulphuration pathways were regulated according to tissue need, and there were some differences in the methionine form.
Assuntos
Galinhas/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Metionina/farmacologia , Ração Animal/análise , Fenômenos Fisiológicos da Nutrição Animal , Animais , Dieta/veterinária , Metionina/análogos & derivados , Metionina/metabolismo , Aumento de PesoRESUMO
We herein report the genetic association between leg problems and bone quality traits in a random mating broiler control population. The leg problem traits were valgus (VL), varus (VR), and tibial dyschondroplasia (TD), and that of bone quality were shank weight (SW), shank length (SL), shank diameter (SDIAM), tibia weight (TW), tibia length (TL), tibia diameter (TDIAM), tibia density (TDEN), tibia breaking strength (TBS), tibia mineral density (TMD), tibia mineral content (TMC), and tibia ash content (TAC). A threshold-linear mixed model, implemented via a Bayesian approach, was employed for the joint analysis of the traits. Genetic correlations of leg problems with bone quality traits ranged from -0.06 to 0.11 suggesting that genetic relationship between leg problems and quality is weak, and management strategies could better alleviate leg problems than genetic improvement.
Assuntos
Densidade Óssea/genética , Mau Alinhamento Ósseo/veterinária , Galinhas , Coxeadura Animal/genética , Osteocondrodisplasias/veterinária , Doenças das Aves Domésticas/genética , Animais , Mau Alinhamento Ósseo/genética , Predisposição Genética para Doença , Membro Posterior/anormalidades , Osteocondrodisplasias/genéticaRESUMO
We report the genetic relationship between growth and bone quality traits in a random mating broiler control population. Traits studied were growth rates from week 0 to 4 [body weight gain (BWG) 0 to 4], from week 0 to 6 (BWG 0 to 6), and residual feed intake (RFI) from week 5 to 6 (RFI 5 to 6). Bone quality traits were obtained at 6 weeks of age. These traits were shank weight (SW), shank length (SL), shank diameter (SDIAM), tibia weight (TW), tibia length (TL), and tibia diameter (TDIAM). Likewise, tibia was used to obtain the tibia density (TDEN), tibia breaking strength (TBS), tibia mineral density (TMD), tibia mineral content (TMC), and tibia ash content (TAC). At the phenotypic level, growth traits were positively correlated with most of the bone quality traits except with TDEN and TAC which tended to show unfavorable associations (-0.04 to -0.31). Heritability of bone quality traits ranged from 0.08 to 0.54. The additive genetic associations of growth traits with weight, length, and diameter of shank and tibia were positive (0.37 to 0.80). A similar pattern was observed with TMD and TMC (0.06 to 0.65). In contrast, growth traits showed unfavorable genetic associations with TDEN, TBS, and TAC (-0.03 to -0.18). It was concluded that bone quality traits have an additive genetic background and they can be improved by means of genetic tools. It appears that selection for growth is negatively correlated with some traits involved in the integrity, health, and maturity of leg bones.
Assuntos
Densidade Óssea/genética , Densidade Óssea/fisiologia , Osso e Ossos/fisiologia , Galinhas/fisiologia , Animais , Fenômenos Biomecânicos/genética , Galinhas/genética , Feminino , MasculinoRESUMO
Improvement in growth has been widely reported as the cause of increased incidence of leg problems in broiler chickens. We report herein the genetic relationship between growth and leg problems in a random mating broiler control population. The traits studied were valgus (VL), varus (VR), and tibial dyschondroplasia (TD), which were expressed on a binary scale of 0 (normal) and 1 (abnormal); growth rates from 0 to 4 wk (BWG 0-4) and from 0 to 6 wk of age (BWG 0-6); and residual feed intake from 5 to 6 wk of age (RFI 5-6). A threshold-linear mixed model was employed for the joint analysis of the categorical and linear traits. Incidences of VL, VR, and TD were 26, 4, and 2%, respectively. Heritability of leg problems ranged from 0.11 to 0.13. Phenotypic correlations alluded to an unfavorable relationship between growth and leg problems; however, the genetic relationship between growth and leg problems was extremely weak, ranging from 0.01 to 0.08. There is, therefore, a basis for genetic improvement in leg problems. However, improved management practices would also be important to reduce incidence of leg problems in broiler chickens.